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10.1007/s12026-012-8371-x

http://scihub22266oqcxt.onion/10.1007/s12026-012-8371-x
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22990458!ä!22990458

suck abstract from ncbi


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pmid22990458      Immunol+Res 2013 ; 55 (1-3): 261-9
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  • The role of Mg2+ in immune cells #MMPMID22990458
  • Brandao K; Deason-Towne F; Perraud AL; Schmitz C
  • Immunol Res 2013[Mar]; 55 (1-3): 261-9 PMID22990458show ga
  • The physiological and clinical relevance of Mg(2+) has evolved over the last decades. The molecular identification of multiple Mg(2+) transporters (Acdp2, MagT1, Mrs2, Paracellin-1, SLC41A1, SLC41A2, TRPM6 and TRPM7) and their biophysical characterization in recent years has improved our understanding of Mg(2+) homeostasis regulation and has provided a basis for investigating the role of Mg(2+) in the immune system. Deletions and mutations of Mg(2+) transporters produce severe phenotypes with more systemic symptoms than those seen with Ca(2+) channel deletions, which tend to be more specific and less profound. Deficiency of the Mg(2+) permeable ion channels TRPM6 or TRPM7 in mice is lethal at embryonic day 12.5 or at day 6.5, respectively, and, even more surprisingly, chicken DT40 B cells lacking TRPM7 die after 24-48 h. Recent progress made in Mg(2+) research has helped to define underlying mechanisms of two hereditary diseases, human Hypomagnesemia (TRPM6 deletion) and X-chromosomal immunodeficiency (MagT1 deletion), and has revealed a potential new role for Mg(2+) as a second messenger. Future elucidation of human Mg(2+) transporters (Mrs2, SLC41A1, SLC41A2, TRPM7) expressed in immunocytes, beyond MagT1 and TRPM6, will widen our knowledge about the potential role of Mg(2+) in the activation of the immune response.
  • |Animals[MESH]
  • |B-Lymphocytes/immunology[MESH]
  • |Cation Transport Proteins/immunology[MESH]
  • |Humans[MESH]
  • |Magnesium/*immunology[MESH]
  • |T-Lymphocytes/immunology[MESH]


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